A new study reveals how viruses that infect bacteria, called bacteriophages or “phages,” use a tiny piece of genetic material to hijack bacterial cells and make more copies of themselves.

The research shows that a very small RNA molecule, called PreS, acts like a hidden “switch” inside the bacterial cell. By flipping this switch, the virus can change how the bacterial cell works and push the infection forward.

Until now, most phage research has focused on viral proteins. This study shows that phages also use RNA molecules to quickly reprogram the host cell after the bacterial genes have already been read and bacterial messages (mRNAs) were made, adding an extra layer of control during infection.

PreS attaches to these important bacterial messages and tweaks them in a way that helps the virus copy its DNA and move more efficiently toward the stage where new viruses are produced and burst out of the cell, killing the bacterium.

Using advanced methods to map RNA–RNA interactions (termed RIL-seq), the researchers found that one of PreS’s key targets is a bacterial message that makes DnaN, a protein that plays a central role in copying DNA. By helping the cell make more DnaN, PreS gives the virus a strong head start in the infection process.

Interestingly, PreS works by changing the shape of the bacterial dnaN message.

Normally, part of this message is tightly folded, which makes it hard for the cell’s protein-making machines (ribosomes) to access. PreS binds to this folded region, opens it up, and allows ribosomes to read and translate the message more efficiently.

A great paper where Miyakawa et al. show attenuation of seizures using chemogenetics for the first time in a nonhuman primate model of epilepsy. I hope chemogenetics moves into clinical trials soon (this paper was published in 2023), it seems very promising as a therapeutic modality. [ https://www.nature.com/articles/s41467-023-36642-6](https://www.nature.com/articles/s41467-023-36642-6)

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Pharmacological and surgical treatments of epilepsy can have unsatisfactory outcomes, so a more targeted and on-demand approach is desirable. Here, the authors demonstrate the usage of inhibitory chemogenetics in male nonhuman primates to attenuate the magnitude and spread of cortical seizures and subsequent body convulsions.

Transposable elements in cancer therapy.

Transposable elements (TEs) are a major source of immunogenic nucleic acids that can be therapeutically reactivated in cancer cells to induce a state of viral mimicry.

TE expression can trigger innate immune sensing pathways, including type I interferon responses, and promote immunogenic cell death via sensors such as RIGI, MDA5, cGAS, and Z-DNA binding protein 1.

Although initially described in the context of epigenetic therapies, viral mimicry is now recognized as a shared response to diverse cancer treatment modalities, including chemotherapies and targeted therapies.

Despite their distinct primary mechanisms, these treatments converge on TE reactivation through disruption of DNA/histone methylation, p53 activation, and perturbation of mRNA splicing.

Therapeutic resistance to chemotherapy, radiation, and targeted agents is associated with TE silencing, identifying TE repression as a targetable axis of resistance.

Combination strategies to induce immunogenic TE expression can further enhance viral mimicry and boost antitumor immunity. https://sciencemission.com/Viral-mimicry-in-cancer-therapy

A new study reveals that bacteria can survive antibiotic treatment through two fundamentally different “shutdown modes,” not just the classic idea of dormancy. The paper is published in the journal Science Advances.

The researchers show that some cells enter a regulated, protective growth arrest, a controlled dormant state that shields them from antibiotics, while others survive in a disrupted, dysregulated growth arrest, a malfunctioning state marked by vulnerabilities, especially impaired cell membrane stability. This distinction is important because antibiotic persistence is a major cause of treatment failure and relapsing infections even when bacteria are not genetically resistant, and it has remained scientifically confusing for years, with studies reporting conflicting results.

By demonstrating that persistence can come from two distinct biological states, the work helps explain those contradictions and provides a practical path forward: different persister types may require different treatment strategies, making it possible to design more effective therapies that prevent infections from coming back.